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Chapter 11 Muscle Tissue Types and Characteristics of Muscular Tissue The Nerve-Muscle Relationship Behavior of Skeletal Muscle Fibers Behavior of Whole.

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Presentation on theme: "Chapter 11 Muscle Tissue Types and Characteristics of Muscular Tissue The Nerve-Muscle Relationship Behavior of Skeletal Muscle Fibers Behavior of Whole."— Presentation transcript:

1 Chapter 11 Muscle Tissue Types and Characteristics of Muscular Tissue The Nerve-Muscle Relationship Behavior of Skeletal Muscle Fibers Behavior of Whole Muscles Muscle Metabolism Cardiac and Smooth Muscle

2 Introduction to Muscle Movement is a fundamental characteristics of all living things Cells capable of shortening & converting the chemical energy of ATP into mechanical energy Types of muscle –skeletal –cardiac –smooth Physiology of skeletal muscle –basis of warm-up, strength, endurance & fatigue

3 Universal Characteristics of Muscle Responsiveness (excitability) –capable of response to chemical signals, stretch or other signals & responding with electrical changes across the plasma membrane Conductivity –local electrical change triggers a wave of excitation that travels along the muscle fiber Contractility -- shortens when stimulated Extensibility -- capable of being stretched Elasticity -- returns to its original resting length after being stretched

4 Skeletal Muscle Voluntary striated muscle attached to bones Muscle fibers (myofibers) as long as 30 cm Exhibits alternating light and dark transverse bands or striations –reflects overlapping arrangement of internal contractile proteins Under conscious control

5 Connective Tissue Elements of Muscle Found between muscle fiber and bone or other attachment –endomysium, perimysium, epimysium, fascia, tendon Not excitable or contractile, but are somewhat extensible & elastic –stretches slightly under tension and recoils when released Called series-elastic components –are connected to each other in linear series –help return muscles to their resting lengths –adds significantly to power output and efficiency of muscles

6 The Muscle Fiber

7 Muscle Fibers (Form follows Function) Multiple flattened nuclei against inside of plasma membrane –due to fusion of multiple myoblasts during development –unfused satellite cells nearby can multiply to produce a small number of new myofibers Sarcolemma has tunnel-like infoldings or transverse (T) tubules that penetrate the cell –carry electric current to cell interior Sarcoplasm is filled with –myofibrils (bundles of parallel protein microfilaments called myofilaments) –glycogen for stored energy & myoglobin binding oxygen Sarcoplasmic reticulum is series of interconnected, dilated, calcium storage sacs called terminal cisternae

8 Thick Filaments Made of 200 to 500 myosin molecules –2 entwined polypeptides (golf clubs) Arranged in a bundle with heads (cross bridges) directed outward in a spiral array around the bundled tails –central area is a bare zone with no heads

9 Thin Filaments Two intertwined strands of fibrous (F) actin –each subunit is a globular (G) actin with an active site Groove holds tropomyosin molecules, each blocking the active sites of 6 or 7 G actins One small, calcium-binding troponin molecule stuck to each tropomyosin molecule

10 Elastic Filaments Huge springy protein called titin (connectin) –runs through core of each thick filament –connects thick filament to Z disc structure Functions –keep thick & thin filaments aligned with each other –resist overstretching –help the cell recoil to its resting length (elasticity)

11 Regulatory & Contractile Proteins Myosin & actin are contractile proteins (they do work) Tropomyosin & troponin are regulatory proteins –act like a switch that starts & stops shortening of muscle cell –the release of calcium into sarcoplasm and its binding to troponin, activates contraction –troponin moves the tropomyosin off the actin active sites

12 Overlap of Thick & Thin Filaments

13 Striations = Organization of Filaments Dark A bands (regions) alternating with lighter I bands (regions) –anisotrophic (A) and isotropic (I) stand for the way these regions affect polarized light A band is thick filament region –lighter, central H band area contains no thin filaments I band is thin filament region –bisected by Z disc protein called connectin, anchoring elastic & thin filaments –from one Z disc (Z line) to the next is a sarcomere I A I

14 Striations and Sarcomeres

15 Relaxed versus Contracted Sarcomere Muscle cells shorten because their individual sarcomeres shorten –pulling Z discs closer together –pulls on sarcolemma Notice neither thick nor thick filaments change length during shortening Their overlap changes as sarcomeres shorten

16 Nerve-Muscle Relationships Skeletal muscle must be stimulated by a nerve or it will not contract (paralyzed) Cell bodies of somatic motor neurons are in brainstem or spinal cord Axons of somatic motor neurons are called somatic motor fibers –each branches, on average, into 200 terminal branches that supply one muscle fiber each Each motor neuron and all the muscle fibers it innervates are called a motor unit

17 Motor Units A motor neuron & the muscle fibers it innervates –dispersed throughout the muscle –when contract together causes weak contraction over wide area –provides ability to sustain long-term contraction as motor units take turns resting (postural control) Fine control –small motor units contain as few as 20 muscle fibers per nerve fiber –eye muscles Strength control –gastrocnemius muscle has 1000 fibers per nerve fiber

18 Neuromuscular Junctions (Synapse) region where a nerve fiber makes a functional connection with its target cell (NMJ) Neurotransmitter (acetylcholine/ACh) released from nerve fiber causes stimulation of muscle cell Components of synapse –synaptic knob is swollen end of nerve fiber (contains ACh) –motor end plate is specialized region of muscle cell surface has ACh receptors on junctional folds which bind ACh released from nerve acetylcholinesterase is enzyme that breaks down ACh & causes relaxation –synaptic cleft = tiny gap between nerve and muscle cells –schwann cell envelopes & isolates NMJ

19 The Neuromuscular Junction

20 Neuromuscular Toxins & Paralysis Pesticides contain cholinesterase inhibitors that bind to acetylcholinesterase & prevent it from degrading ACh –spastic paralysis & possible suffocation –minor startle response can cause death Tetanus or lockjaw is spastic paralysis caused by toxin of Clostridium bacteria –blocks glycine release in the spinal cord & causes overstimulation of the muscles Flaccid paralysis with limp muscles unable to contract caused by curare that competes with ACh –respiratory arrest

21 Electrically Excitable Cells (muscle & nerve) Plasma membrane is polarized or charged –resting membrane potential is due to Na+ outside of cell and K+ & other anions inside of cell –difference in charge across the membrane is potential inside is slightly more negative (-90 mV) Plasma membranes exhibit voltage changes in response to stimulation –ion gates open allowing Na+ to rush into cell and then K+ to rush out of cell (quick up-and-down voltage shift is called action potential) –spreads over cell surface as nerve signal or impulse

22 Muscle Contraction & Relaxation Four actions involved in this process –excitation where action potentials in the nerve lead to formation of action potentials in muscle fiber –excitation-contraction coupling refers to action potentials on the sarcolemma activate myofilaments –contraction is shortening of muscle fiber or at least formation of tension –relaxation is return of fiber to its resting length Images will be used to demonstrate the steps of each of these actions

23 Excitation of a Muscle Fiber

24 Excitation (steps 1 & 2) Nerve signal stimulates voltage-gated calcium channels that result in exocytosis of synaptic vesicles containing ACh = ACh release

25 Excitation (steps 3 & 4) Binding of ACh to the surface of muscle cells opens Na+ and K+ channels resulting in an end- plate potential (EPP)

26 Excitation (step 5) Voltage change in end-plate region (EPP) opens nearby voltage-gated channels in plasma membrane producing an action potential

27 Excitation-Contraction Coupling

28 Excitation-Contraction Coupling (steps 6&7) Action potential spreading over sarcolemma reaches and enters the T tubules -- voltage-gated channels open in T tubules causing calcium gates to open in SR

29 Excitation-Contraction Coupling (steps 8&9) Calcium released by SR binds to troponin Troponin-tropomyosin complex changes shape and exposes active sites on actin

30 Contraction (steps 10 & 11) Myosin ATPase in myosin head hydrolyzes an ATP molecule, activating the head and cocking it in an extended position It binds to an active site on actin

31 Contraction (steps 12 & 13) Power stroke = shows myosin head releasing the ADP & phosphate as it flexes pulling the thin filament along With the binding of more ATP, the myosin head releases the thin filament and extends to attach to a new active site further down the thin filament –at any given moment, half of the heads are bound to a thin filament, preventing slippage –thin and thick filaments do not become shorter, just slide past each other (sliding filament theory) 12. Power Stroke; sliding of thin filament over thick

32 Relaxation (steps 14 & 15) Nerve stimulation ceases and acetylcholinesterase removes ACh from receptors so stimulation of the muscle cell ceases

33 Relaxation (step 16) Active transport pumps calcium from sarcoplasm back into SR where it binds to calsequestrin ATP is needed for muscle relaxation as well as muscle contraction

34 Relaxation (steps 17 & 18) Loss of calcium from sarcoplasm results in troponin- tropomyosin complex moving over the active sites which stops the production or maintenance of tension Muscle fiber returns to its resting length due to stretching of series-elastic components and contraction of antagonistic muscles

35 Rigor Mortis Stiffening of the body beginning 3 to 4 hours after death -- peaks at 12 hours after death & diminishes over next 48 to 60 hours Deteriorating sarcoplasmic reticulum releases calcium Activates myosin-actin cross bridging & muscle contracts, but does not relax. Muscle relaxation requires ATP & ATP production is no longer produced after death Fibers remain contracted until myofilaments decay

36 Length-Tension Relationship Amount of tension generated depends on length of muscle before it was stimulated –length-tension relationship (see graph next slide) Overly contracted (weak contraction results) –thick filaments too close to Z discs & cant slide Too stretched (weak contraction results) –little overlap of thin & thick does not allow for very many cross bridges too form Optimum resting length produces greatest force when muscle contracts –central nervous system maintains optimal length producing muscle tone or partial contraction

37 Length-Tension Curve

38 Muscle Twitch in Frog Experiment Threshold is minimum voltage necessary to produce action potential –a single brief stimulus at that voltage produces a quick cycle of contraction & relaxation called a twitch (lasting less than 1/10 second) Phases of a twitch contraction –latent period (2 msec delay) only internal tension is generated no visible contraction occurs since only elastic components are being stretched –contraction phase external tension develops as muscle shortens –relaxation phase loss of tension & return to resting length as calcium returns to SR A single twitch contraction is not strong enough to do any useful work

39 Recruitment & Stimulus Intensity Stimulating the whole nerve with higher and higher voltage produces stronger contractions More motor units are being recruited –called multiple motor unit summation –lift a glass of milk versus a whole gallon of milk Maximal recruitment

40 Production of Variable Contraction Strengths Stimulating the nerve with higher voltage get stronger contractions because recruit more motor units Stimulate the muscle at higher frequencies (stimuli/sec) –up to 10, produces twitch contractions with full recovery between twitches – , each twitch develops more tension than the one before (treppe) due to failure to remove all Ca+2 – , each stimulus arrives before the previous twitch is over temporal or wave summation produces incomplete tetanus – , no time to relax between stimuli so twitches fuse into smooth prolonged contraction called complete tetanus (normal smooth movements)

41 Production of Variable Contraction Strengths (1) Twitch and Treppe Contractions Stimulating a muscle at variable frequencies –low frequency (up to 10 stimuli/sec) each stimulus produces an identical twitch response –moderate frequency (between stimuli/sec) each twitch has time to recover but develops more tension than the one before (treppe or staircase phenomenon) –calcium was not completely put back into SR –heat of tissue increases myosin ATPase effeciency (warm-up exercises)

42 Production of Variable Contraction Strengths (2) Incomplete and Complete Tetanus Higher frequency stimulation (20-40 stimuli/second) generates gradually more strength of contraction –each stimuli arrives before last one recovers temporal summation or wave summation –incomplete tetanus = sustained fluttering contractions Maximum frequency stimulation (40-50 stimuli/second) –muscle has no time to relax at all –twitches fuse into smooth, prolonged contraction called complete tetanus –rarely occurs in the body

43 Isometric & Isotonic Contractions Isometric muscle contraction –develops tension without changing length Isotonic muscle contraction –tension development while shortening = concentric –tension development while lengthening = eccentric

44 Muscle Contraction Phases Isometric & isotonic phases of lifting a heavy box Tension builds even though the box is not moving Then muscle begins to shorten & maintains the same tension from then on

45 ATP Sources All muscle contraction depends on ATP Pathways of ATP synthesis –anaerobic fermentation (ATP production limited) occurs without oxygen, but produces toxic lactic acid –aerobic respiration (far more ATP produced) requires continuous oxygen supply, produces H2O & CO2

46 Muscle Immediate Energy Needs In a short, intense exercise (100 m dash), oxygen need is supplied by myoglobin Most ATP demand is met by transferring P i from other molecules (phosphagen system) –myokinase transfers P i groups from one ADP to another, converting the latter to ATP –creatine kinase obtains Pi groups from creatine phosphate and donates them to ADP to make ATP Result is power enough for 1 minute brisk walk or 6 seconds of sprinting

47 Muscle Short-Term Energy Needs Once phosphagen system is exhausted, glycogen- lactic acid system (anaerobic fermentation) takes over – produces ATP for seconds of maximum activity –muscles obtain glucose from blood & stored glycogen –while playing basketball or running around baseball diamonds

48 Muscle Long-Term Energy Needs After 40 seconds of exercise, respiratory & cardiovascular systems catch up and begin to deliver enough oxygen for aerobic respiration –oxygen consumption rate increases for first 3-4 minutes & then levels off to a steady state –ATP production keeps pace with demand Limits are set by depletion of glycogen & blood glucose, loss of fluid and electrolytes through sweating –little lactic acid buildup occurs

49 Fatigue Fatigue is progressive weakness & loss of contractility from prolonged use Causes –ATP synthesis declines as glycogen is consumed –ATP shortage causes sodium-potassium pumps to fail to maintain membrane potential & excitability –lactic acid lowers pH of sarcoplasm inhibiting enzyme function –accumulation of extracellular K+ lowers the membrane potential & excitability –motor nerve fibers use up their acetylcholine

50 Endurance Ability to maintain high-intensity exercise is determined by maximum oxygen uptake and nutrient availability –VO 2 max is proportional to body size, peaks at age 20, is larger in trained athlete & males –depends on the supply of organic nutrients fatty acids, amino acids & glucose carbohydrate loading is used by some athletes –dietary strategy used to pack glycogen into muscle cells –may add water at same time (2.7 g water with each gram/glycogen) –side effects include heaviness feeling

51 Oxygen Debt Need to breathe heavily after strenuous exercise –known as excess postexercise oxygen consumption (EPOC) –typically about 11 liters extra is consumed Purposes for extra oxygen –replace oxygen reserves (myoglobin, blood hemoglobin, in air in the lungs & dissolved in plasma) –replenishing the phosphagen system –reconverting lactic acid to glucose in kidneys and liver –serving the elevated metabolic rate that occurs as long as the body temperature remains elevated by exercise

52 Slow- and Fast-Twitch Fibers Not all muscle fibers are metabolically alike, but all fibers of a single motor unit are similar Slow oxidative, slow-twitch fibers –more mitochondria, myoglobin & capillaries –adapted for aerobic respiration & resistant to fatigue –soleus & postural muscles of the back (100msec/twitch) Fast glycolytic, fast-twitch fibers –rich in enzymes for phosphagen & glycogen-lactic acid systems –sarcoplasmic reticulum releases calcium quickly so contractions are quicker (7.5 msec/twitch) –extraocular eye muscles, gastrocnemius and biceps brachii Proportions of different muscle types determined genetically = born sprinter

53 Types of Muscle Fibers

54 Strength and Conditioning Factors that increase strength of contraction –muscle size and fascicle arrangement –size of motor units and motor unit recruitment –frequency of stimulations, length of muscle at start of contraction and fatigue Resistance training (weight lifting) –stimulates cell enlargement due to synthesis of more myofilaments -- some cell splitting may occur Endurance training (aerobic exercise) –produces an increase in mitochondria, glycogen & density of capillaries

55 Cardiac Muscle Cells are shorter, thicker, branched and linked to each other at intercalated discs –electrical gap junctions allow cells to stimulate their neighbors & mechanical junctions keep the cells from pulling apart –sarcoplasmic reticulum is less developed but T tubules are larger to admit Ca+2 from extracellular fluid –damaged cells repaired by fibrosis, not mitosis Autorhythmic due to pacemaker cells Uses aerobic respiration almost exclusively –large mitochondria make it resistant to fatigue –very vulnerable to interruptions in oxygen supply

56 Smooth Muscle Fusiform cells with one nucleus –30 to 200 microns long & 5 to 10 microns wide –no visible striations, sarcomeres or Z discs –thin filaments attach to dense bodies scattered throughout sarcoplasm & on sarcolemma –SR is scanty & has no T tubules calcium for contraction comes from extracellular fluid If present, nerve supply is autonomic –releases either ACh or norepinephrine –different effects in different locations

57 Types of Smooth Muscle Multiunit smooth muscle –in largest arteries, iris, pulmonary air passages, arrector pili muscles –terminal nerve branches synapse on individual myocytes in a motor unit –independent contraction Single-unit smooth muscle –in most blood vessels & viscera as circular & longitudinal muscle layers –electrically coupled by gap junctions –large number of cells contract as a unit

58 Stimulation of Smooth Muscle Involuntary & contracts without nerve stimulation –hormones, CO2, low pH, stretch, O2 deficiency –pacemaker cells in GI tract are autorhythmic Autonomic nerve fibers have beadlike swellings called varicosities containing synaptic vesicles –stimulates multiple myocytes at diffuse junctions

59 Features of Contraction and Relaxation Calcium triggering contraction is extracellular –enters cell through channels triggered by voltage, hormones, neurotransmitters or stretching of the cell calcium ion binds to calmodulin -- activates myosin light-chain kinase which activates the myosin head with ATP to bind actin -- power stroke occurs when hydrolyzes 2nd ATP Thin filaments pull on intermediate filaments attached to dense bodies on the plasma membrane –shortens the entire cell in a twisting fashion Contraction & relaxation very slow in comparison –slow myosin ATPase enzyme & slow pumps that remove Ca+2 Uses l0-300 times less ATP to maintain the same tension –latch-bridge mechanism maintains tetanus (muscle tone) keeps arteries in state of partial contraction (vasomotor tone)

60 Contraction of Smooth Muscle Cells

61 Responses to Stretch Stretch opens mechanically-gated calcium channels causing muscle response –food entering the esophagus brings on peristalsis Stress-relaxation response necessary for hollow organs that gradually fill (urinary bladder) –when stretched, tissue briefly contracts then relaxes Must contract forcefully when greatly stretched –thick filaments have heads along their entire length –no orderly filament arrangement -- no Z discs Plasticity is ability to adjust tension to degree of stretch such as empty bladder is not flabby

62 Muscular Dystrophy Group of hereditary diseases in which skeletal muscles degenerate & are replaced with adipose Mainly a disease of males –appears as child begins to walk –rarely live past 20 years of age Normal allele makes dystrophin, a protein that links actin filaments to cell membrane –absence of dystrophin leads to torn cell membranes Fascioscapulohumeral MD -- facial & shoulder muscle only

63 Myasthenia Gravis Autoimmune disease where antibodies attack NMJ and bind ACh receptors together in clusters –fibers remove the receptors –less and less sensitive to ACh drooping eyelids and double vision difficulty swallowing weakness of the limbs respiratory failure Disease of women between ages of 20 and 40 Treated with cholinesterase inhibitors, thymus removal or immunosuppressive agents

64 Myasthenia Gravis Drooping eyelids and weakness of muscles of eye movement

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